[Retracted] Rivaroxaban attenuates thrombosis by targeting the NF-κB signaling pathway in a rat model of deep venous thrombus

Ma, Ji; Li, Xinxi; Wang, Yang; Yang, Zhenwei; Luo, Jia

doi:10.3892/ijmm.2018.3565

Cited by 3 publications

(1 citation statement)

References 43 publications

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“…Many researchers have confirmed the potential anti-inflammatory role of RVX. The previous studies of Jhaveri et al (2011), Basile et al, 2012and his colleagues in 2012, Ma et al, 2018and his coworkers in 2017, and Al-Harbi et al (2020 were in line with the above-discussed literature that RVX has anti-inflammatory effects. Also, RVX dampened the inflammatory response in the ischemic brain (Dittmeier et al, 2016).…”

Section: Discussionsupporting

confidence: 79%

Rivaroxaban Modulates TLR4/Myd88/NF-Kβ Signaling Pathway in a Dose-Dependent Manner With Suppression of Oxidative Stress and Inflammation in an Experimental Model of Depression

et al. 2021

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Depression is a common mental illness leading to upset or anxiety, with a high incidence rate in the world. Depression can lead to suicidal thoughts and behavior. The present study aimed to evaluate the effect of the direct oral anticoagulant rivaroxaban (RVX), in the model of depression induced by chronic unpredicted mild stress (CUMS) in rats. Fifty-six male Wister rats were randomly divided into seven experimental groups (8 rats/group); Group 1: Control group given vehicle per oral (p.o.), Group 2: RVXL-control group (received rivaroxaban 20 mg/kg/day, p.o..), Group 3: RVXH-control group (received rivaroxaban 30 mg/kg/day, p.o.), Group 4: chronic unpredictable mild stress (CUMS) group, Group 5: FLX-treated CUMS group (received fluoxetine 10 mg/kg/day, p.o..), Group 6: RVXL-treated CUMS group (received rivaroxaban 20 mg/kg/day, p.o.), and Group 7: RVXH-treated CUMS group (received rivaroxaban 30 mg/kg/day, p.o.). The rats received the drugs from the first day of the experiment and continued till 4 weeks—the duration of the study. The following were measured: monoamine neurotransmitters, malondialdehyde (MDA), total nitrite/nitrate (NOx), reduced glutathione (GSH), superoxide dismutase (SOD), Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), nuclear factor‐kappa B (NF‐κB), tumor necrosis factor-α (TNF-α), brain-derived neurotrophic factor (BDNF), and vascular endothelial growth factor-A (VEGF-A). A forced swimming test (FST) was done. Furthermore, histological changes and glial fibrillary acidic protein (GFAP) immunoexpression were evaluated. CUMS showed a significant decrease in hypothalamic neurotransmitters, hippocampal GSH, SOD, BNDF, and VEGF-A with a significant increase in hippocampal MDA, NOx, NF-kβ, Myd88, TLR4, TNF-α, and GFAP immunoexpression. RVX showed significant improvement in all parameters (p-value < 0.0001). In conclusion, RVX in a dose-dependent manner possesses potent ameliorative effects against depression by reducing the oxidative stress and inflammatory process, through the regulation of the TLR4/Myd88/NF-kβ signaling pathway.

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Section: Discussionsupporting

confidence: 79%

Rivaroxaban Modulates TLR4/Myd88/NF-Kβ Signaling Pathway in a Dose-Dependent Manner With Suppression of Oxidative Stress and Inflammation in an Experimental Model of Depression

et al. 2021

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Role of NF-κB in Platelet Function

Kojok

El-Kadiry

Merhi

2019

IJMS

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Platelets are megakaryocyte-derived fragments lacking nuclei and prepped to maintain primary hemostasis by initiating blood clots on injured vascular endothelia. Pathologically, platelets undergo the same physiological processes of activation, secretion, and aggregation yet with such pronouncedness that they orchestrate and make headway the progression of atherothrombotic diseases not only through clot formation but also via forcing a pro-inflammatory state. Indeed, nuclear factor-κB (NF-κB) is largely implicated in atherosclerosis and its pathological complication in atherothrombotic diseases due to its transcriptional role in maintaining pro-survival and pro-inflammatory states in vascular and blood cells. On the other hand, we know little on the functions of platelet NF-κB, which seems to function in other non-genomic ways to modulate atherothrombosis. Therein, this review will resemble a rich portfolio for NF-κB in platelets, specifically showing its implications at the levels of platelet survival and function. We will also share the knowledge thus far on the effects of active ingredients on NF-κB in general, as an extrapolative method to highlight the potential therapeutic targeting of NF-κB in coronary diseases. Finally, we will unzip a new horizon on a possible extra-platelet role of platelet NF-κB, which will better expand our knowledge on the etiology and pathophysiology of atherothrombosis.

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Protective effect of rivaroxaban on arteriosclerosis obliterans in rats through modulation of the toll‑like receptor 4/NF‑κB signaling pathway

Lou

Yang

et al. 2019

Exp Ther Med

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The aim of the present study was to explore the pharmacological role of rivaroxaban in rats with arteriosclerosis obliterans (ASO) and the potential mechanism of its action. A total of 60 adult male Sprague Dawley (weighing 210–250 g) were randomly assigned into either the sham group, model group or Riv group. Rats in the sham group were fed a normal diet, whereas those in model group and Riv group were fed a high-fat diet for 8 weeks. After establishment of the ASO model, rats in the Riv group were intragastrically administered 10 mg/kg rivaroxaban, whereas those in the sham group and the model group were administrated with the same volume of 0.9% saline for 4 weeks. At the end of animal procedures, a blood sample and the femoral artery of the rats were harvested. The results of the present study revealed that rats in the model group presented with an irregularly narrowed femoral artery lumen, disordered endothelial cells, internal elastic plates and smooth muscle cells. By comparison, the arterial wall structure and stenosis of the femoral artery of rats in Riv group recovered and all the pathological changes were alleviated after rivaroxaban treatment. Levels of total cholesterol, triglycerides and low-density lipoproteins decreased, whereas the level of high-density lipoproteins increased in the Riv group compared with the model group. Rivaroxaban treatment significantly reduced serum levels of interleukin-1, tumor necrosis factor-α and monocyte chemoattractant protein-1 (MCP-1), and increased the serum level of transforming growth factor-β (TGF-β). Rats in the Riv group had reduced expression of toll-like receptor 4 (TLR4), NF-κB and MCP-1, and increased expression of TGF-β in femoral artery tissues compared with the model group. Therefore rivaroxaban may have exerted its anti-atherosclerotic effects by regulating the expression of genes in the TLR4/NF-κB signaling pathway and the activation of the downstream molecules.

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[Retracted] Rivaroxaban attenuates thrombosis by targeting the NF-κB signaling pathway in a rat model of deep venous thrombus

Cited by 3 publications

References 43 publications

Rivaroxaban Modulates TLR4/Myd88/NF-Kβ Signaling Pathway in a Dose-Dependent Manner With Suppression of Oxidative Stress and Inflammation in an Experimental Model of Depression

Rivaroxaban Modulates TLR4/Myd88/NF-Kβ Signaling Pathway in a Dose-Dependent Manner With Suppression of Oxidative Stress and Inflammation in an Experimental Model of Depression

Role of NF-κB in Platelet Function

Protective effect of rivaroxaban on arteriosclerosis obliterans in rats through modulation of the toll‑like receptor 4/NF‑κB signaling pathway

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